Biologists have identified several hormones that play a key role in eating and the way our body uses energy and stores fat. These hormones include cortisol, insulin, leptin, and ghrelin. In spite of research that shows that these hormones let us know when we are hungry and when we have had enough food, there is still doubt as to their role in obesity.
Another theory is that obesity may be the result of a genetic predisposition. It seems that body size runs in families. Having one obese parent results in a 40 percent chance of becoming obese, and having two obese parents increases the likelihood of becoming obese to 80 percent.
One biological theory of over-eating and obesity is that there is an imbalance of hormones. As you will see in the chart below, there are several hormones that play a role in our eating behavior. Being able to isolate a single hormone to argue that it plays a key role in obesity has not yet been possible. It is highly likely that all of these hormones may play a key role and even more likely that there is some level of interaction between the hormones.
Cortisol is secreted by the adrenal cortex in response to stress via the hypothalamic-pituitary-adrenal (HPA) axis. It increases blood glucose levels and mobilizes energy stores. However, chronically high cortisol levels can lead to increased appetite and fat accumulation, particularly in the abdominal region. This is because cortisol promotes lipogenesis (fat storage) and inhibits lipolysis (fat breakdown), contributing to central obesity, which is linked to metabolic disorders.
Ghrelin is produced mainly by the stomach’s gastric cells and acts on the hypothalamus to stimulate hunger. It also slows down fat metabolism, promoting fat storage. While ghrelin levels typically rise before meals and fall after eating, individuals with higher body weight paradoxically have lower baseline ghrelin levels. This suggests that ghrelin is more involved in meal initiation rather than long-term regulation of body weight.
Insulin, produced by pancreatic β-cells, facilitates the uptake of glucose into cells and promotes glycogen storage in the liver. In obesity, prolonged exposure to high insulin levels can lead to insulin resistance, where cells fail to respond effectively. This impairs glucose uptake, causing hyperglycemia and increased fat storage. Elevated insulin levels also inhibit lipolysis, making it harder for the body to burn fat, thereby perpetuating obesity.
Leptin is secreted by adipocytes (fat cells) and signals the hypothalamus to reduce appetite. It regulates energy balance by inhibiting hunger and promoting energy expenditure. However, in obesity, leptin resistance can occur, where the hypothalamus becomes less sensitive to leptin signals. This leads to a failure in recognizing satiety, causing overeating despite high leptin levels. The exact mechanisms behind leptin resistance remain unclear, though chronic inflammation in adipose tissue may play a role.
Ghrelin levels are lower in individuals with a higher body weight compared with lean individuals, which suggests ghrelin could be involved in the long-term regulation of body weight. One would expect higher levels in people with obesity. However, ghrelin levels are usually lower in people with higher body weight compared with lean people, which suggests ghrelin is not a cause of obesity but may influence eating behaviors that may contribute to obesity.
High levels of cortisol can, for example, increase appetite with a preference for “comfort food” and cause white adipose (fat) tissue to redistribute to the abdominal region, which may ultimately lead to abdominal obesity.
Ghrelin is secreted by the stomach and is often called the "hunger hormone." Ghrelin tells the hypothalamus that you are hungry and that you need to eat. High levels of ghrelin are associated with over-eating and obesity.
Insulin is a hormone secreted by the pancreas that allows your body to use glucose from carbohydrates in the food that you eat for energy or to store glucose for future use. Insulin resistance is when the body does not respond appropriately to insulin, leading to type II diabetes. There is a correlation between insulin resistance and obesity.
Leptin is secreted by adipose tissue (fat cells) and tells the hypothalamus that we have had enough to eat. Leptin resistance is thought to play a role in obesity.
Ghrelin tells us that we need to eat. When glucose levels in the blood fall, ghrelin levels rise, telling the brain that we need to eat to get more energy. Could this hormone play a role in obesity?
Interestingly, ghrelin levels are lower in individuals with a higher body weight compared with lean individuals, which suggests ghrelin could be involved in the long-term regulation of body weight. One would expect higher levels in people with obesity. However, ghrelin levels are usually lower in people with higher body weight compared with lean people, which suggests ghrelin is not a cause of obesity but may influence eating behaviors that may contribute to obesity.